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Journal of Virology, July 2001, p. 6070-6085, Vol. 75, No. 13
0022-538X/01/$04.00+0   DOI: 10.1128/JVI.75.13.6070-6085.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Hantavirus Infection Induces the Expression of RANTES and IP-10 without Causing Increased Permeability in Human Lung Microvascular Endothelial Cells

J. Bruce Sundstrom,1,* Laura K. McMullan,2 Christina F. Spiropoulou,2 W. Craig Hooper,3 Aftab A. Ansari,1 Clarence J. Peters,2,dagger and Pierre E. Rollin2

Department of Pathology and Laboratory Medicine, Emory University School of Medicine, Atlanta, Georgia 30323,1 and Special Pathogens Branch2 and Division of AIDS, STD, and TB Laboratory Research,3 National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia 30333

Received 12 December 2000/Accepted 28 March 2001

Sin Nombre virus (SNV) and Hantaan virus (HTN) infect endothelial cells and are associated with different patterns of increased vascular permeability during human disease. It is thought that such patterns of increased vascular permeability are a consequence of endothelial activation and subsequent dysfunction mediated by differential immune responses to hantavirus infection. In this study, the ability of hantavirus to directly induce activation of human lung microvascular endothelial cells (HMVEC-Ls) was examined. No virus-specific modulation in the constitutive or cytokine-induced expression of cellular adhesion molecules (CD40, CD54, CD61, CD62E, CD62P, CD106, and major histocompatibility complex classes I and II) or in cytokines and chemokines (eotaxin, tumor necrosis factor alpha, interleukin 1beta [IL-1beta ], IL-6, IL-8, MCP-1, MIP-1alpha , and MIP-1beta ) was detected at either the protein or message level in hantavirus-infected HMVEC-Ls. Furthermore, no virus-specific enhancement of paracellular or transcellular permeability or changes in the organization and distribution of endothelial intercellular junctional proteins was observed. However, infection with either HTN or SNV resulted in detectable levels of the chemokines RANTES and IP-10 (the 10-kDa interferon-inducible protein) in HMVEC-Ls within 72 h and was associated with nuclear translocation of interferon regulatory factor 3 (IRF-3) and IRF-7. Gamma interferon (IFN-gamma )-induced expression of RANTES and IP-10 could also be detected in uninfected HMVEC-Ls and was associated with nuclear translocation of IRF-1 and IRF-3. Treatment of hantavirus-infected HMVEC-Ls with IFN-gamma for 24 h resulted in a synergistic enhancement in the expression of both RANTES and IP-10 and was associated with nuclear translocation of IRF-1, IRF-3, IRF-7, and NF-kappa B p65. These results reveal a possible mechanism by which hantavirus infection and a TH1 immune response can cooperate to synergistically enhance chemokine expression by HMVEC-Ls and trigger immune-mediated increases in vascular permeability.

* Corresponding author. Mailing address: Department of Pathology and Laboratory Medicine, Winship Cancer Institute, Room B4337, Emory University School of Medicine, Atlanta, GA 30322. Phone: (404) 778-4564. Fax (404) 778-5016. E-mail: JSUNDST{at}emory.edu.

dagger Present address: Department of Pathology, University of Texas Medical Branch, Galveston, TX 77555.

Journal of Virology, July 2001, p. 6070-6085, Vol. 75, No. 13
0022-538X/01/$04.00+0   DOI: 10.1128/JVI.75.13.6070-6085.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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